Skepticism

EVENTS

αEP: Complexity is not usually the product of selection

This is another addition to my αEP series about evolutionary psychology. Here’s the first, and unfortunately there are several more to come.

By the way, people are wondering about the α in the title. Don’t you people do any immunology? α is standard shorthand for “anti”.

I mentioned in the last one this annoying tendency of too many pro-evolution people to cite “complexity” as a factor that supports the assertion of selection for a trait. Strangely, the intelligent design creationists also yell “Complexity!” at the drop of a hat, only it’s to prove that evolution can’t work.

They’re both wrong.

I ran across a prime example of this recently in a post by John Wilkins (It’s pick-on-John-Wilkins day! Hooray!)

Opponents, largely following Gould and Lewontin’s 1979 attack, tend to assert (often without consideration of the particular attempts to give adaptive explanations) that any and all adaptive hypotheses are cheap and to be avoided. This has the effect of basically eliminating natural selective accounts of anything. But we know that selection is the only process that results in complexity over any time, and the fact there are complex traits among organisms leads to the inevitable conclusion that we should be able to give selective explanations from time to time. I have argued before that we should think of adaptation as a viable hypothesis at all times; but being viable doesn’t make it true. The problem is not that EP or sociobiology makes adaptive hypotheses. They should. It is that they often make them without testing them.

I will concede the general point: a well-designed and testable adaptive hypothesis is a perfectly reasonable starting point to do science, and I agree that one big problem with evolutionary psychology is that most of their adaptive hypotheses are poorly done. But I’ve highlighted the chunk in the middle that’s just absurd: complex traits are the product of selection? Come on, John, you know better than that. Even the creationists get this one right when they argue that there may not be adaptive paths that take you step by step to complex innovations, especially not paths where fitness doesn’t increase incrementally at each step. Their problem is that they don’t understand any other mechanisms at all well (and they don’t understand selection that well, either), so they think it’s an evolution-stopper — but you should know better.

This is the trap Michael Behe falls into, too. It’s the assumption that you have to have an adaptive scenario for every step, and an inability to imagine non-adaptive solutions. I think if selection were always the rule, then we’d never have evolved beyond prokaryotes — all that fancy stuff eukaryotes added just gets in the way of the one true business of evolution, reproduction.

So let’s work through a hypothetical scenario of increasing complexity, and you try to see where selection is essential. And then I’ll give some real world examples.

Imagine an enzyme E with with a fairly nonspecific, broad spectrum of binding for various chemical substrates. It can bind substrate A or substrate B with equal facility, and then carries out some modification of the substrate — let’s say it hydrolizes some side group. We’ll call this enzyme EAB for its substrates.

Now imagine a fairly common mutational event, a gene duplication. An individual in this population acquires a second copy of its gene, so now it is EAB-EAB. Is this event dependent on selection? No, obviously not.

But now this mutation spreads through the population, so a significant fraction of the individuals carry it. Is that dependent on selection?

That’s because in many other cases, the duplication is going to be neutral in effect, or even deleterious. It’s going to be a tiny cost in replication, for example (but negligible, because selection doesn’t see very small fitness costs and replication is a small part of most cell’s energy budget), and many processes are sensitive to dosage, where increases in gene number can damage the equilibrium of the cell. If this weren’t true, then Down syndrome children, who carry an extra copy of a whole chromosome, would be superhuman.

So let’s say that this step of the increasing frequency of a gene duplication is usually going to be the result of genetic drift, but sometimes will have an adaptive benefit…but you have to demonstrate the latter, rather than assuming it.

So now you have a population with a large subset carrying the EAB-EAB duplication. What next? Mutations can occur in either of the copies.

The most likely result is destruction of the function of one of the copies: EAB-EAB becomes EAB-X, where X is now a damaged, non-functional pseudogene. We’re back to square one, except of course if you were arguing that the duplication had to incur a benefit, because now the pseudogene is nothing but cost — it incurs that neglible replication cost, but also it would be at a disadvantage relative to those individuals that carried your hypothetically advantageous duplication. But look: the human genome contains at least 12,000 pseudogenes (out of 20,000 genes), and some genes, like cytochrome C, may have 49 pseudogene copies. Most of these mutations are also going to be nearly neutral.

The interesting case, though, is where something changes in one of the copies short of actually destroying the gene. What if one loses it’s broad specificity and now becomes able only to bind one of the substrates…for example, we now have an individual carrying EA-EAB. Will this variant expand through the population by selection?

Again, not likely. This individual is still processing A and B with a pair of enzymes, and any difference between it and others would be small (and probably invisible to selection, at least if it’s in a messy slow breeding metazoan, for instance).

Similarly, there would be other mutations in the population: we could have mutants carrying EAB-EB, for instance, with a more specific second enzyme. We could have mutants that knock out functions in any order: X-EAB, or EB-EAB. All kinds of variants arise by chance mutation, and spread to varying degrees through the population by drift. No selection need be involved, and you get all this complexity in the population arising entirely spontaneously. And a good part of the reason that this can occur is because selection plays no role.

Things get more complex in the absence of selection. Selection, as Wilkins well understands, is generally a conservative process that removes phenotypic variation from the population (with some exceptions). It is precisely the inability of selection to cull all variants that deviate from the successful, well-tested norm that allows novel complexity to emerge.

In our hypothetical population, for instance, we have all kinds of different patterns of the E gene: we have the ancestral type, EAB, the duplicated form, EAB-EAB, forms carrying pseudogenes, X-EAB and EAB-X, and forms with subtle differences in the specificity of the enzymes, EA-EAB and EAB-EB. None of this is the product of selection. But now you can get recombination, and maybe some of those combinations will be visible to selection.

For instance, when X-EAB breeds with EAB-X, some of the progeny could be X-X, a complete knockout of the enzyme. That could be, but isn’t necessarily, deleterious. You could get the particularly interesting combination EA-EB, where now what you’ve accomplished is the separation of two of the functions of the ancestral enzyme into two separate, more specific enzymes.

Is the condition EA-EBmore fit than the ancestral state of EAB? I would argue that usually, no, it’s not. It’s going to be a nearly neutral variant in that both individuals process the A and B molecules just fine. Maybe somewhere further down the road, two separate molecules to do these two functions opens the door to more flexibility and interesting new possibilities, but evolution and selection do not care about future potential, only with short term consequences.

The bottom line is that you cannot easily explain most increases in complexity with adaptationist rationales. You have to consider chance as far more important, and far more likely to produced elaborations.

Do these phenomena operate in the real world, rather than just hypothetical scenarios? Yes. For example, look at the globin genes. These are found in two clusters, an α cluster with seven genes (including two pseudogenes) and a β cluster with five genes. All the genes are related and similar and function — these are all proteins with heme and oxygen-carrying functions — where each gene has slightly different functions (one may have a higher affinity for oxygen than another) and patterns of expression (one may be expressed at a different stage of development than another, or in a different range of tissues), and we can see specific functional adaptations for each, but their origin has to be in a selectively neutral condition.

A fetal hemoglobin with a high affinity for oxygen is an adaptation when expressed in a fetus, but detrimental when expressed in a pregnant woman (it wouldn’t share oxygen as readily with the fetus). The selective advantage could only arise after the different globins had evolved, and when differential gene expression mechanisms had been coupled to them to assure that they would only be expressed under appropriate conditions. The origin was not a selection event, but the refinement to specific roles probably was.

In his posts about our paper, Behe’s first error is to ignore the fact that adaptive combinations of mutations can and do evolve by pathways involving neutral intermediates. Behe says that if it takes more than one mutation to produce even a crude version of the new protein function, then selection cannot drive acquisition of the adaptive combination.

This does not mean, however, that the evolutionary path to the new function is blocked or that evolution runs into a “brick wall,” as Behe alleges. If the initial mutations have no negative effect on the ancestral function, they can arise and hang around in populations for substantial periods of time due to genetic drift, creating the background in which an additional mutation can then yield the new function and be subject to selection. This is precisely what we observed in our studies of the evolution of the glucocorticoid receptor (GR).

In our 2007 paper in Science, we showed that multiple mutations were indeed required for the GR to evolve its specificity for the hormone cortisol; some of the mutations that trigger the change in function are deleterious if introduced in isolation, but others are “permissive”: they have no apparent effect on the function of the protein, but once they are in place the protein can tolerate the other mutations that shift and then optimize the new function.

Even in something as specific as the physiological function of a biochemical pathway, adaptation isn’t the complete answer, and evolution relies on neutral or nearly neutral precursor events to produce greater functional complexity.

patrickhertal… please note that the quote should be “…TOO many pro-evolution people…”, not “…MANY pro-evolution people…”. One such person may be “too many”… is John Wilkins not a pertinent example?

I personally know several individuals who would absolutely qualify as “pro-evolution” and who routinely make similar claims, but they’re neither well-known enough for you to recognize their names nor likely to appreciate me listing their names here. Ask around, I’m sure you can fine a few people who are both “pro-evolution” and don’t have a complete understanding of all the underlying mechanisms that can be involved in changing populations over time.

Even people who should know better can get sloppy. An underlying assumption in too many (note the “TOO” again, please) biology courses and working laboratories is that every change that sticks in a population must be “adaptive” or “advantageous”.

Evolutionary psychologists some years back proposed that there are certain clues one can use to suggest that something is an adaptation, and one of those was “complexity.” If a thing is complex, it must have arisen through selection because randomness does not lead to complexity. However, what we see as complexity might not really be adaptive complexity, but rather, the simple fact that living stuff is complex, so even a simple (hypothetical) adaptation is going to be embedded in complexity somehow. Also, it may be the case that some Evolutionary Psychologist have skipped a step: If complexity leads one to consider something adaptive, as a clue to suggest that one develop a hypothesis about it, fine. But to lead to concluding that it is adaptive is wrong.

So complexity might be a clue toward determining adaptivity, but it shouldn’t claim to answer the question.

PZ, its not entirely clear that your molecular enzyme example really makes a good comparison to the development of a mental process. (Maybe that’s another strike against EP, actually, not for it.) Do we have any reason to think they are in any way analogous at all? Wouldn’t traditional neurology and psychology argue that our brains can construct complex mental frameworks, using very basic building blocks? Or is that not even related?

Opponents, largely following Gould and Lewontin’s 1979 attack, tend to assert (often without consideration of the particular attempts to give adaptive explanations) that any and all adaptive hypotheses are cheap and to be avoided.

He’s not going to cite or quote any, though. And that wasn’t Gould and Lewontin’s argument. They recommended a pluralistic approach, “abandoning exclusive focus on the adaptationist programme.”

So sociobiology as a hypothesis is acceptable. It need not lead to Nazism, racism, sexism or US exceptionalism.

I’m not familiar with either person, but it’s a bit hard to believe that John Wilkins and/or Ed Clint would deny the importance of genetic drift. Was genetic drift an important mechanism behind the evolution of the human brain, for instance? From what I’ve read over the last few years, Wilkins and Clint would be crazy to suggest otherwise. Perhaps they’ll respond at some point to your characterization of their views.

Secondly, I don’t see how your (excellent) argument here about the reality of genetic drift casts any new aspersions on the field of evolutionary psychology. If EP researchers are ignoring genetic drift as an explanation for complexity, then obviously they deserve your criticism.

I know it takes time to write these kinds of posts, so let me once again express my appreciation for the free online education.

I am looking forward to the rest of this series on the specifics of evolution and populations. We tend to think in hard edges and distinct categories and this post helps to make the distinctions we think we see blur a little.
That blurring is very disturbing to “just so” stories and our convenient categories.

Wouldn’t traditional neurology and psychology argue that our brains can construct complex mental frameworks, using very basic building blocks? Or is that not even related?

Don’t know. The fact that they can do that wouldn’t explain how that happens or how it originated.

I’m a bit confused too, pretty much any time “complexity” enters the discussion. It’s not clear to me what that’s supposed to mean in this context. I don’t think it could be anything like “cannot be made of simple parts,” because apparently nothing would fit that description. It’s more like “the simple parts have many different properties or relationships with one another,” right?

I’m not familiar with either person, but it’s a bit hard to believe that John Wilkins and/or Ed Clint would deny the importance of genetic drift.

Maybe we could get past what people are supposedly “denying” or not denying, and just keep track of what their arguments rest on. They may not have really thought through the implications of some of the premises and may not really believe they are true, yet there they are in print so that is what we have to deal with (if that is in fact the case in this instance). You don’t need people going around denying stuff outright, for those kinds of mistakes to happen.

Wouldn’t traditional neurology and psychology argue that our brains can construct complex mental frameworks, using very basic building blocks?

Maybe, but that sounds more metaphorical and conceptually categorical than useful in terms of evolved traits. I may be making an incorrect assumption from definitions of what you mean by “mental building blocks” though. Also, mental frameworks don’t evolve in the biological sense, populations of organisms do. So yes, an entirely different thing.

So complexity might be a clue toward determining adaptivity, but it shouldn’t claim to answer the question.

Complexity is evidence of something being complex. Adaptivity doesn’t necessarily require complexity, complexity doesn’t imply (non/)adaptivity or selection. The specifics of some complex thing may be specific clues regarding that thing. Complexity in and of itself is irrelevant to the argument.

I may be wrong on this, but it just feels like that should end with ‘us for instance’ , or ‘humans for instance’. or not have for instance in there at all.

Why? Any slow-reproducing metazoan counts. Besides, EP is so human-focused, I would personally make obvious avoidance of a “like us” comparison in discussion of EP if possible. Not sure about PZ – I’m not him.

Maybe we could get past what people are supposedly “denying” or not denying, and just keep track of what their arguments rest on.

Your comment here is essentially tone-trolling, and therefore quite hypocritical seeing that it resides on Pharyngula, the ancestral home of “Fuck-you and btw here’s my argument.” May I assume you’re leveling this chastisement at PZ as well? Consider it discarded as worthless.

Every comment you direct at me, in fact, seems to suggest some sort of personal insecurity on your part. Why don’t you take your own advice, and leave this kind of stuff out, or better yet, simply ignore my comments? Input like this doesn’t move us any closer to the truth in matters pertaining to biology or science.

Listen. I’ll take you out to the driving range, and watch you try to hit a few golf balls. Then, after laughing my ass off at your incompetence, I’ll suggest that you simply don’t understand anything about golf. This will constitute a perfect analogy for how I’m treated in here by the likes of you.

I enjoy learning, and that’s why I read and participate on PZ’s blog. Learning takes practice, and much trial and error, whether it is in sports, or in evolutionary biology. If you can’t understand this simple fact, then I suggest you buy a set of golf clubs and demonstrate this to yourself.

Wouldn’t traditional neurology and psychology argue that our brains can construct complex mental frameworks, using very basic building blocks? Or is that not even related?

consciousness razor replied:

Don’t know. The fact that they can do that wouldn’t explain how that happens or how it originated.

I’m a bit confused too, pretty much any time “complexity” enters the discussion. It’s not clear to me what that’s supposed to mean in this context. I don’t think it could be anything like “cannot be made of simple parts,” because apparently nothing would fit that description. It’s more like “the simple parts have many different properties or relationships with one another,” right?

I don’t think I conveyed my thought very well: what I meant to ask was, to what degree are our brains “flexible abstract thinking engines”, as opposed to “interconnected function-specific logic units”? Because more than anything, it sounds like Evolutionary Psychology is strongly supportive of the latter.

Now to be clear, I know that regions of the brain are dedicated to large areas such as vision, language, motor control, abstract thought, etc. But within the abstract reasoning portion, do we really have “specialized neural circuits” for each and every different kind of decision? That seems… implausible.

Or maybe I’m just revealing my ignorance of the current state of brain science?

as Wilkins well understands, is generally a conservative process that removes phenotypic variation from the population (with some exceptions). It is precisely the inability of selection to cull all variants that deviate from the successful, well-tested norm that allows novel complexity to emerge.

are you saying Wilkins is unaware that selection->fixation is a simplistic version of how selection actually works?

or are you saying that Wilkins just explains it in simple terms.

and how does this have anything to do with Evo Psych?

are you trying to say evo psych follows simplistic models of selection, and is unaware, as an entire discipline, of the thousands of papers published demonstrating that selection is just part of the things that adjust frequency within populations?

Your entire evo-psych series sounds remarkably like Gould’s arguments in Spandrels, and can be critiqued in exactly the same way.

maybe if you actually took apart specific examples? But so far, I can’t find much scientific merit in your attacks on the discipline as a whole.

No, it’s not. There was nothing about tone in it. If you thought there was, then you misunderstood.

You said it’s hard to believe that John Wilkins and/or Ed Clint would deny the importance of genetic drift. And you’re right, that is hard to believe. But as far as I can see, no one has claimed that they would. So you’ve made an irrelevant point.

To understand whether they’re speaking accurately, though, it might be worthwhile to keep track of what their arguments rest on — for instance, to note anything overlooked — rather than assuming that they overlooked something because they explicitly, consciously deny its importance.

I’m also arguing that this mistaken attachment to selection as the only relevant mechanism for evolution (even when they do pay lip service to drift) permeates EP, and makes most EP work foundationally invalid.

Good thing I lack time to Marjonovic this one; it is a bizarre post.
It has nothing whatsoever to do with EP in the first place.
“Too many pro-evolution people” apparently = Clint and Wilkins.
“Complexity” has been re-defined to mean one aspect of genomic complexity, basically the existence of gene families.
These are fine examples of genomic complexity originating by duplication, drift, and mutation. But even leaving aside the downplayed importance of selection in spreading, fixing, and maintaining these genetic systems: So what?

Clint for one explicitly talked about “complex organs”. Organs, not number of related geres. Do you mean to imply that it’s a straight extrapolation from two copies of a fake enzyme to a freaking brain? As for Wilkins, he’s a philosopher and almost certainly had a specific meaning in mind when he used the term “complexity”–you could have asked him. I bet it wasn’t five different hemoglobin subunits. Presumably it had something to do with whatever neural complexity is necessary to cause behavioral patterns. (It’s worth noting that nobody in the discussion at any level has any clue about how behavior and its underlying neural substrates are genetically encoded, even for a simple stereotyped behavior like spider web-spining. None. That’s the problem with Nerd’s show-me-the-gene bullshit.)

And come on. Nobody thinks that natural selection is the origin of genetic variation. Who are you even arguing with?

PZ, its not entirely clear that your molecular enzyme example really makes a good comparison to the development of a mental process. (Maybe that’s another strike against EP, actually, not for it.) Do we have any reason to think they are in any way analogous at all? Wouldn’t traditional neurology and psychology argue that our brains can construct complex mental frameworks, using very basic building blocks? Or is that not even related?

Oh~

It’s true that there is a general perception of mental processes being too vague and complex to be subjected to the same rules as other organismal traits, and this is a common misconception in psychology and, yes, neuro(bio)logy.

I must admit that the biological basis of behavior is one of my favourite topics and something I personally enjoy teaching and discussing IRL, even though I’m a neuropathologist by training.

Here are three biologically illustrative examples of the real plasticity of behavior:

Giant square eggs

Animal behavior may seem to be almost perfectly adapted to the daily life of animals, but it really shows its inner plasticity by subjecting the animals to a new environment. This is perfectly illustarted in a now classic experiment, where behaviorists Baerends and Kruijt studied the egg rolling behavior of sea gulls. Nesting sea gulls display an innate tendency to roll any stranded eggs they find in their surroundings towards their nest. Baerends et al tested the specificity of this behavior by exposing the birds to several fake eggs of differing sizes, colours and shapes. Surprisingly, even though sea gull eggs are relatively small and.. round, the animals showed an increasing preference towards huge green eggs(sea gull eggs are not green) and, even more strikingly, the best results were obtained by exposing the birds to giant square eggs. This hidden variability was completely masked by the conventional environment these birds lived in, in spite of the very existence of the neural mechanisms underpining this seemingly maladaptive behavior.

There’s no way on earth this behavior was actually selected for o.O

A mental map

In mammals and birds, the hippocampal formation in the brain directs the storage and retrieval of declarative memory aswell as the perception and representation of spatial location. Basically, this formation is a “listener” of other brain areas, receiving continuous updates of brain activity and sending feedback messages to modify and strengthen the conenctions between these areas. Long story short, the brain sends messages by synchronizing neuron activity between distant areas so that neurons spiking in different areas can “wire together”. The hippocampus has its own slower synchronization rythm(theta) locked to the activity of the faster rythms relaying otehr areas, allowing the readout of these activities and the later reinforcement of intracortical connections, what we know as “memory”.

But memory formation isn’t the oldest function of this formation. In fact, these rythms and synchronizations weren’t discovered by looking at memory, they were discovered by studying the neural representation of spatial location in rats! Spatial location is also based in inter-areal synchronization and uses the same mechanisms as memory, albeit being an older function of the hippocampal formation.

An interesting hypothesis formulated by Buzsáki et al is that the hippocampal was first an organ devoted to spatial location, only to be later co-opted into a map to navigate in not only spatial, but mental coordinates.

Magic trichromatism

Most people, even scientists, assume that new mental capacities require a complex amount of adaptive changes in brain structure to appear. Recent studies in transgenic animals show how the addition of a single gene can drive the appearance of a new perceptual construct. Most mammals, including a fair share of primates, are dichromatic, seeing only in green and blue. New world monkeys were able to perceive red colour when the gene coding for old world monkey red proteins was introduced into their genome. Now, you’ll say, both monkeys are quite related, so their mental mechanisms may be similar, but the same result was achieved by introducing this gene into rodents (last common ancestor 80 million years ago) and confirmed by operant codnitioning!

These are just three examples showing the astounding plasticity and hidden capacity of our nervous system. I personally think that even more amazing findings concering the variability, plasticity and capacity for change and adaptation in this system are yet to come.

But as far as I can see, no one has claimed that they would. So you’ve made an irrelevant point.

It wasn’t an irrelevant point, because I’ll bet dollars to doughnuts it is precisely what Wilkins and Clint would (will?) say in their own defense. Taking one specific sentence out of the more general context comprised by a biologist’s entire body of work seems a bit disingenuous. It’s cherry-picking, plain and simple.

@PZ in #23:

Thanks for the clarification. I’ll assume your statement about “permeating EP” to be an accurate characterization, because I have no evidence to the contrary, although I’m sure there are EP researchers who will disagree with you.

It wasn’t an irrelevant point, because I’ll bet dollars to doughnuts it is precisely what Wilkins and Clint would (will?) say in their own defense.

Great. Nevertheless, to understand whether they’re speaking accurately, though, it might be worthwhile to keep track of what their arguments rest on — for instance, to note anything overlooked — rather than assuming that they overlooked something because they explicitly, consciously deny its importance.

That’s all about keeping track of substance, not tone. :)

Taking one specific sentence out of the more general context comprised by a biologist’s entire body of work seems a bit disingenuous. It’s cherry-picking, plain and simple.

You’ve misunderstood again. If such a sentence was used to say “look! this person denies the importance of genetic drift!” then that would be cherrypicking.

If such a sentence was used to say “when making this here particular argument, this person is underestimating the importance of genetic drift”, then focusing on that particular argument can be appropriate.

You are splitting hairs. The entire series is named “Anti-EP” (using the letter alpha), fer chrissakes! Would that I had the time to keep up with everything Wilkins and Clint say — I don’t. I rely instead upon people like PZ Myers and Jerry Coyne to give me the straight scoop.

Unfortunately, I’d also have to suggest that this series of articles has a secondary function as some sort of defense of Rebecca Watson’s latest misadventure, but I know how unpopular that argument will be in here.

Is it OK to name a pro-evolution person here who makes mistakes like selection => complexity? Tim Minchin. And just about any popular figure without a scientific background. Standup and musical comedians may be in force here, but I’d say that many of those on “our side” create, blog and network (and irl network) about these topics while getting some things wrong.

It’s like the whole Al Gore climate warming film debacle. Why doesn’t everyone worldwide just accept scientific findings and understand them in depth without having to have it bludgeoned into their heads through years of education?

Maybe we could get past what people are supposedly “denying” or not denying, and just keep track of what their arguments rest on.

Your comment here is essentially tone-trolling

Your comment is essentially false, and you are essentially a ridiculous jackass.

Every comment you direct at me, in fact, seems to suggest some sort of personal insecurity on your part.

As far as I know, I’ve directed two, one today and the other yesterday. I can’t see how either suggests any such thing. Honestly, if I hadn’t already known you were a trolling asshole, I’d be surprised by how insecure your responses in this thread seem to be.

Secondly, I don’t see how your (excellent) argument here about the reality of genetic drift casts any new aspersions on the field of evolutionary psychology. If EP researchers are ignoring genetic drift as an explanation for complexity, then obviously they deserve your criticism.

Do most evolutionary psychologists consider neutral evolution as the null hypothesis and then reliably quantify fitness or selection coefficients in order to reject it? Do they look for the signatures of selection in the genome (looking for selective sweeps or nonsynonymous change rates in candidate genes for instance) or in population variability? These are correct and effective ways to take into account gentic drift.

Some of these things cannot be studied in humans of course, but they can be studied in model animals, something animal psychologists are perfectly suited and able to do.

Your hypothesis isn’t worth much as long as you don’t reject the genetic drift null hypothesis.

what I meant to ask was, to what degree are our brains “flexible abstract thinking engines”, as opposed to “interconnected function-specific logic units”? Because more than anything, it sounds like Evolutionary Psychology is strongly supportive of the latter.

Fascinating question! I’d honestly say that the former is an emergent property of the latter. The basic concept here is that our perception works at a different timescale than our fine brain activity. Consider a film, it is in fact composed of a discontinuous set of images projected fast enough so that our brain thinks it is really a continuous scene. This is a consequence and a reflection of how our brain works, as our perception “binds” together an amazing amount of interconnected phenomena into a continuous percept. A film is perceived as continous when its fps is over 25, while our brain works at around 80 cycles per second.

Now to be clear, I know that regions of the brain are dedicated to large areas such as vision, language, motor control, abstract thought, etc. But within the abstract reasoning portion, do we really have “specialized neural circuits” for each and every different kind of decision? That seems… implausible.

It indeed is an implausible conclusion. We don’t have specific circuits for every decision, but we have something way better, an entire organ dedicated to creating decision rules based on experience: the basal ganglia and reward circuits. No need for specific circuits when you have an organ that can bind together signals from different areas and associate them through a logical rule (based or not on actual reward).

It’s worth noting that nobody in the discussion at any level has any clue about how behavior and its underlying neural substrates are genetically encoded, even for a simple stereotyped behavior like spider web-spining. None. That’s the problem with Nerd’s show-me-the-gene bullshit.

Oh c’mon Chas, you know very well that single genes don’t encode behavior, it’s the genetic, protein-level and cellular interactions plus the environment what causes changes in behavior. It is mostly a question of polygenic inheritance and complex genetic architecture, but we can show that changes in single genes are able to unfold into measurable changes in behavior. Either in my previous opsin example or in another example of transgenic animals: mice carrying the human version of transcription factor FoxP2, here’s the abstract:

It has been proposed that two amino acid substitutions in the transcription factor FOXP2 have been positively selected during human evolution due to effects on aspects of speech and language. Here, we introduce these substitutions into the endogenous Foxp2 gene of mice. Although these mice are generally healthy, they have qualitatively different ultrasonic vocalizations, decreased exploratory behavior and decreased dopamine concentrations in the brain suggesting that the humanized Foxp2 allele affects basal ganglia. In the striatum, a part of the basal ganglia affected in humans with a speech deficit due to a nonfunctional FOXP2 allele, we find that medium spiny neurons have increased dendrite lengths and increased synaptic plasticity. Since mice carrying one nonfunctional Foxp2 allele show opposite effects, this suggests that alterations in cortico-basal ganglia circuits might have been important for the evolution of speech and language in humans.

As a plus, they used a gene both related to behavior and having underwent measurable natural selection in humans(!)

I don’t think I conveyed my thought very well: what I meant to ask was, to what degree are our brains “flexible abstract thinking engines”, as opposed to “interconnected function-specific logic units”? Because more than anything, it sounds like Evolutionary Psychology is strongly supportive of the latter.

Now to be clear, I know that regions of the brain are dedicated to large areas such as vision, language, motor control, abstract thought, etc. But within the abstract reasoning portion, do we really have “specialized neural circuits” for each and every different kind of decision? That seems… implausible.

That’s what de Waal argues in the article Chas linked to the other day. I’m bothered by comparisons with organs or genes, complex or otherwise, because the modularity business is fundamentally different. Discussing psychological phenomena as “modules” and traits is just reifying abstractions.

Anyway, do you understand yet why #16 was about keeping track of substance, not tone? Or are you still confused about that as well?

I’m not confused one bit, but more importantly, this point you’re attempting to pursue doesn’t interest me in the slightest. Sorry to be so blunt, but you’re boring me. I’d rather spend my precious time learning about biology, not listening to superficial defenses of the rampant cronyism that permeates Pharyngula.

If you weren’t so damn insecure, you wouldn’t resort to these kinds of tactics. Run along now.

Bullshit. What exactly am I supposed to be insecure about? Give me your very best internet diagnosis.

Also, once you’ve sorted that out, why are you acting as if being “insecure” is itself a bad thing? Are we supposed to be “secure” all the time? Should we generally treat insecurity as if it were some kind of insult?

I’m not confused one bit, but more importantly, this point you’re attempting to pursue doesn’t interest me in the slightest. Sorry to be so blunt, but you’re boring me.

You shouldn’t have come up with that bullshit, if you didn’t want it to be discussed. Anyway, no one gives a fuck if you stop reading. You don’t have to fucking advertise your boredom, since you’re here voluntarily.

I’d rather spend my precious time learning about biology, not listening to superficial defenses of the rampant cronyism that permeates Pharyngula.

Either you don’t know what “cronyism” means, or PZ needs to explain why none of us have cushy new offices yet.

You’ve got some kind of axe to grind, but I’d need to meet you in person before I could figure out what it is.

And btw I’m a mechanical engineer, not a biologist. Would the old saying “Pick on somebody your own size” be something you can wrap your head around? I’m telling you right now I’m not one bit interested in your commentary. Please direct it somewhere else, preferably to somebody who will give you the biological comeuppance you so obviously need.

Maybe we could get past what people are supposedly “denying” or not denying, and just keep track of what their arguments rest on. They may not have really thought through the implications of some of the premises and may not really believe they are true, yet there they are in print so that is what we have to deal with (if that is in fact the case in this instance). You don’t need people going around denying stuff outright, for those kinds of mistakes to happen.

Pick a quote from the above and explain how it constitutes either tone trolling and/or a cry for attention.

I can’t lead your way, since I don’t see how you could possibly get to there from here, but if you’re scared then I will at least hold your hand.

The best way for someone like you to improve yourself, is to challenge people who are your superiors. As much as I would like to inhabit such a position, I’m afraid my background and training simply wouldn’t suffice. May I suggest you direct your comments on biology to Professor Myers, for example?

Now, if you were thinking of taking up golf on the other hand, I assure you I wouldn’t treat you in the disgusting and patronizing manner you continue to display in here. I wouldn’t even laugh (much) at you.

Swim, dude. Challenge yourself. Make the best of your time on this planet, instead of directing snarky, insult-ridden garbage at people who are only trying to learn and enjoy PZ’s lively blog.

I’m trying to help you learn, nhbu. I’ve proposed an exercise in backing up your unfounded assertions. See #48. If you try actually making a case for those assertions, you’ll challenge yourself and maybe grow your intellectual capabilities. Mind, you won’t learn how to win an argument today, but it will at least be an exercise.

Actually, you have a reply to virtually anything anyone says, whether or not it’s relevant, correct, or even interesting. You are merely an attention-seeking dweeb, who uses the internet as a shield to prevent the kinds of responses that are truly merited in cases like these.

Honestly, I’m like this offline too, and it rarely leads to violence as you insinuate. Regardless, you’re confused again. It’s not your assertions about me that I’m suggesting you ought to back up. Quote from #16 and try arguing that one of the things you’ve claimed about it is true.

I don’t have to call anybody out at you insistence. In fact, if you make that claim, what they said was probably true,otherwise you would present evidence yourself.. You are the hypocrite, and the lurkers know that. Your continuing presence without an argument proves that. If you have a point, make it. If you don’t have a point, which is the case, shut the fuck up. Losers and liars and bullshitters can’t put up, and can’t shut up. Like you.

In Ed Clint’s post “What is Evolutionary Psychology” back in August I take bring up the complexity issue with him.

Ed Clint:

I didn’t say that all change is natural selection. I said that it’s the only explanation there is for complex features…This is an uncontroversial observation from evolutionary biology that I extend to complex behaviors dependent upon sophisticated neural development.”

And so I’d like to raise an additional point. The relatively simplicity of recombinations or copy-number variation means that complexity at the level of a trait doesn’t imply complex underlying genetics, so it’s not hard to see how drift can have a role in variation. The issue isn’t whether it arose randomly, which is trivially obvious and is likely a straw-man argument PZ’s making, but how it became fixed…Ed Clint for one doesn’t seem to care much about the underlying genetics and mechanisms involved. What’s lacking from either side is a discussion on how “complex traits/features” become fixed. A discussion of the effects of drift and natural selection on phylogenetic reconstructions would be a good place to start, but it’s likely over our collective heads.

I think the larger problem for Ed (and I realize he’s probably no authority in EP) is that populations are rarely if ever perfectly optimized for their environment so it’s always problematic reverse-engineering environmental scenarios under which various traits arose.

Ed’s non-answer

The nature of selection is that organisms are adapted to conditions in the past. Therefore, the conditions of the past are relevant to understanding present organisms. We could not understand why whales have hipbones without knowing their environment in the past was the land. You are free to search for a drift explanation if you wish.

The following tells me that Ed needs to brush up on the genetics whether he cares about it or not.

For example, let’s say you’re correct about the FOXP2 etc.., coinciding with the expansion of the neocortex. Why was there neocortex to begin with? Why was there cortex? Why was there a FOXP2 gene to be modified? These things all did not exist at one time, and later they did. By random drift? I think not….To be honest, I’m not really interested in this argument.

because he doesn’t understand it. But there is hope.

The paper I authored concluded that some 3 decades of research into an adaption fails to prove that the trait is in fact an adaptation. When such a conclusion is reached, I might look for the answer at the mechanism level, perhaps at the level of genes or molecules

This comment section is cracking me up. I wrote an essay dissecting this very subject for a philosophy of biology course. Once again, this recent drama has convinced me that even vocal internet atheists who consider themselves scientifically literate haven’t been paying as much attention as they might like to think. The appeal to complexity even has a name: adaptationism. It’s a product of a gene-centered view of evolution. This is what the whole evo-devo vs. adaptationism debate is about. Clint’s FAQ that he linked to went on and on about how complexity implies selection. Dude, even Dawkins is an adaptationist. Frankly, I don’t think Dawkins is that relevant to evolutionary biology as a field anymore but he’s a big name and is hardly someone obscure. He is a major public figure advocating evolutionary biology, after all.

Either way, PZ is not launching some kind of a straw-argument here. Adaptationism is way more common than it should be. Here, enjoy this talk by Kirschner who discusses some alternatives to pure adaptationist views: http://vimeo.com/10466831

Some people define insanity as trying the same thing over and over again…

Yep, your continued posts prove your insanity.

Ugh. Both of you, please quit it with that. 1) that was always a stupid, lazy definition of insanity; 2) it’s just unfair to people with mental illnesses, who are as likely to attempt new solutions as anyone else.

Gillt, if I’m going to be honest with you, I have no idea what your point is actually supposed to be. Adaptationists argue that natural selection is the only way that complex traits can evolve. That is what they’re appealing to. They have a bunch of other assumptions too but I think the complex traits = natural selection is what PZ is getting at. While natural selection is definitely capable of promoting complex traits, it is hardly the only way they can arise. If people wander around assuming everything that is complex must also be adaptive they end up inflating their false positive rate and leads to attempts to explain selective advantages of traits where none may actually exist.

Thank you for this anti-EP information. It’s very interesting and I’m looking forward to the next installment. But aside from the specific mechanisms that might or might not be involved, I’m a bit confused about where EP diverges from the normal speculation about how humans evolved.

As an example, the standard narrative claims that humans are by nature monogamous, and that monogamous marriage is universal in human culture. But there seems to be considerable physical evidence that we evolved in poly-amorous groups. Is it legitimate to look at body dimorphism, for example, and note that apes with a larger difference in size between male and female tend to be apes that have one dominant male commanding the sexual favors of a harem of females? When I was in university it was claimed that the gorilla was doomed because it is simply undersexed and has too small a penis and testicles, ignoring the possibility that you don’t need a big dick and huge balls if you can beat the crap out of the other males. Humans have testicles that are intermediate between gorillas and chimps. Is it legitimate to assume from this fact that we may have evolved in groups where a certain amount of multi-partner sex was common female behavior? Similarly, many apes (Or maybe they are monkeys. I get confused about this stuff) rely on huge testicles and voluminous ejaculate to flush the semen of rivals from the female’s vagina (these guys have balls like grapefruit), but it has been noted that the glans of the human penis is shaped in such a way that it sucks out rival sperm from the vagina. Is it EP to think that this might indicate that we evolved in groups where such an adaptation benefited our genes? This is, after all, a testable hypotheses to the extent that scientists have created artificial ejaculate and used an artificial vagina and a dildo to test how much was removed by repeated strokes of the dick.

Does this kind of speculation fall under the category of EP? Is it legitimate to ask whether, since we did most of our evolving before the huge cultural change that was agriculture, we might not be hard wired for behavior that was common before we all got so sedentary and women became more like chattel, and that this might be messing with our societal hopes and desires now? Is this EP?

The relatively simplicity of recombinations or copy-number variation means that complexity at the level of a trait doesn’t imply complex underlying genetics, so it’s not hard to see how drift can have a role in variation.

It actually goes both ways, you can’t just happily sum the complexity of different levels in a living being and expect the result to be additive. The opposite is also true, a seemingly simple trait can have enormously complex underlying genetics.

The issue isn’t whether it arose randomly, which is trivially obvious and is likely a straw-man argument PZ’s making, but how it became fixed…

This is not what is being discussed in here. This is a discussion concerning not the origin, but the existence of unselected variability in populations. Genetic drift is about the genetic makeup of populations over time, not how this variability arose in the first place. This what Kimura wrote in 1983(emphasis mine):

The neutral theory also asserts that most of the intraspecific variability at the molecular level, such as is manifested by protein polymorphism, is essentially neutral, so that most polymorphic alleles are maintained in the species by mutational input and random extinction. In other words, the neutral theory regards protein and DNA polymorphisms as a transient phase of molecular evolution and rejects the notion that the majority of such polymorphisms are adaptive and maintained in the species by some form of balancing selection

(it is important to understand that at the time this was written, the study of the molecular basis of complex traits was still in its infancy, which explains Kimura’s reluctance to sway outside the realm of DNA and proteins)

Ed Clint for one doesn’t seem to care much about the underlying genetics and mechanisms involved.

He should. This is old stuff, but years, no, decades ago the whole field agreed that only an understanding of both the ultimate(evolutionary, population-level) and proximate(mechanisms) causes of behavior could account for a correct and complete explanation of behavior. Of course, this also goes both ways when mechanistic studies make silly claims without checking the evolutionary basis of what they are studyingin the first place.

What’s lacking from either side is a discussion on how “complex traits/features” become fixed.

Ahhh, the essentialist fallacy. A common error of experimentalists. Most behavioral traits aren’t fixed at all, they actually show quite a lot of variability in wild populations. Taking aside humans, in which behavioral diversity is quite easy to imagine, let’s talk about some animal examples.

Reducing variability is actually the main point of most laboratory experiments with animals, which means that these animals are subjected to a controlled, repeatable and standardized environment. This actually hides their inherent behavioral plasticity and genetic diversity.

A sizeable number of published literature on artificial selection in lab mice, ranging from nest building behaviors to social ones, shows that there is a hidden underlying substrate of molecular variation affecting behavioral traits in mice populations. It is difficult to imagine how such variation would be maintained by natural selection, especially taking into account that these mouse strains have been kept in controlled captivity for a very long number of generations.

For instance, I’m quoting the discussion section of an article by Koteja et al. (1999) to highlight just how behavior-specific this genetic variation can be(again, emphasis mine):

In other words, the effect of our phenotypic selection protocol has beenrather specific for running in wheels (or attempting to run in locked wheels). This suggests that the genes and neurophysiological pathways controlling voluntary wheel-running behaviour are largely independent of
those controlling other behaviours (at least of those studied), and that wheel running can evolve independently of other behaviours.

As prof. Myers said before, if behavioral traits had been fixed by strong selection, this variabilty would be reduced of insignificant instead of being selectable.

I think the larger problem for Ed (and I realize he’s probably no authority in EP) is that populations are rarely if ever perfectly optimized for their environment so it’s always problematic reverse-engineering environmental scenarios under which various traits arose.

I wholeheartedly agree on the reverse-engineering problem, it is technically very difficult (not to say impossible) to identify the past evolutionary causes leading to the selection of a trait. Not only the environment is completely different, the genetic background of the animal population has drastically changed aswell.

That’s being overly dramatic but I agree with you here and it’s because I wasn’t at all clear. I should have said how the alleles become fixed and not the actual behaviors. Which is also why I disagree with this statement:

you can’t just happily sum the complexity of different levels in a living being and expect the result to be additive.

Sure, epistasis…I mean what else could you be implying? But you don’t know this because it’s an open question as to what role epistasis plays in shaping complex traits. The alternative is the multiple small additive effects model*, the effect of common SNPs say, which, for example, explains some of the heritability of human height and even in complex behaviors such as fear phenotypes. A better understanding of penetrance will reveal why a variant (common or rare) results in a phenotypic trait. And we aren’t there yet.

This is not what is being discussed in here. This is a discussion concerning not the origin, but the existence of unselected variability in populations. Genetic drift is about the genetic makeup of populations over time, not how this variability arose in the first place. This what Kimura wrote in 1983(emphasis mine):

I think the post was about both and if we are to take the post in its intended context–as an anti-EP polemic–then the origin stuff is a strawman.

here is a hidden underlying substrate of molecular variation affecting behavioral traits in mice populations. It is difficult to imagine how such variation would be maintained by natural selection

Well obviously not in inbred mouse lines kept in captivity but there’s no reason why variation in genetic architecture among phenotypes, generally, isn’t shaped by selection.

The “behavioral trait” in question is wheel-running propensity after decades of inbreeding and confinement in small plastic cages. This is not a “trait” that could possibly be selected (or even be expressed) in a wild population. It only had a causal link to fitness after the experimenters made up their fake environment of artificial selection. It’s a crappy, crappy example.

If body size was adaptive, would we predict zero variation in body size?

I would predict that body size variation would be inversely proportional to the strength of the selecting force(s). If body size were already tightly bounded, you wouldn’t have as much variation in body size to “select” from in future generations.

would predict that body size variation would be inversely proportional to the strength of the selecting force(s).

That’s one simplistic possibility. Unless it’s the variation itself being selected. Consider lower than expected dissimilarity in the MHC loci of some populations because what was being selected for was not predicted correctly. It’s more reasonable to hypothesize that for some populations assortative mating patterns suggest an optimal, rather than maximal, number of MHC alleles as the driving force of selection.

“selection is the only process that results in complexity over any time”

I think over any time might be defensible. It is one thing to specify a mechanism for generation of standing or cryptic genetic variation by a combination of macro- and micro- mutations. This comes under evolvability, I guess (and can lead into the arguments as to whether evolvability is selected for). It is another to quantify the amounts of phenotypic complexity generated by neutral or nearly neutral processes that persist over long periods of time, as opposed to being just as easily lost by further mutation. If the “usual” outcome for a gene duplication is a pseudogene, then we still need selection, as inferred in your lovely amylase example.

Sigh, you’re right. I had considered “fixed” behavior as a singular rather than the result of a multiplex of responses. Shortly after posting, I realized that compensatory traits could maintain variability despite selection apparently acting upon a lone trait. I wasn’t familiar with MHC in this context, looks like it’s time to do more reading!

This looks to me like a great summary of the objections to selection-heavy EP hypotheses.

Except that none of the phenomena listed get in the way of complex adaptations, they just make it much more difficult for interested human scientists to figure out the genetic underpinnings of such adaptations.

But, you have not quantified complexity, let alone say when there was an increase in it in the hypothetical example you give. If you don’t do this, you can’t talk about the evolution of complexity; it becomes a guessing game what we are talking about, and there is no chance that everyone will think of complexity as the same thing.

On top of that, there seems to be no distinction made anywhere between ‘complexity’ and ‘complex traits’. They need not be the same thing. Without defining complexity here(!), I’ll say that complexity can indeed easily arise by neutral processes, whereas complex traits cannot (but does have neutral and random processes involved) – it requires selection. And with that you’re going to ask me for a definition of a trait, so here is one: A single measurable component of the phenotype that has a function.

The key word here is function, without which I don’t know of any that can evolve without selection. Not selection every step of the way, as random processes are required (at least that’s how it occurs in nature), but selection at some point. The moment the trait acquires function, it becomes selected for.

On the other hand, ‘genomic complexity’ may not describe the state of a trait, but rather is the idea that the genome has many components that are intricately connected – which can arise by neutral processes.

“The key word here is function, without which I don’t know of any that can evolve without selection. ”

Evolution is just the change in genetic frequency of alleles over time. There is nothing in there that says you need selection for the frequencies to change. Not only that but as pointed out above if selection pressures are very small then randomness will still win out.

Say a different eye colour in fruit flies, a gene breaks so that an enzyme is no longer transcribed and you have a second eye colour (because the enzyme no longer changes the structure of the eye pigment. The flies don’t care about the eye colour in mating and the fact that the resources to transcribe that enzyme are no longer used gives this new eye colour a slight advantage. Nothing else is affected. Then that small gain in resources from the cells in the eye no longer making 1 enzyme are so small to the overall energy balance of the fly that the benefit is incredibly small. In the end chance and genetic drift could lead this to fixation or remove it from the gene pool. Either way you have evolution with little to no selection involved. If you don’t trust me go brush up on your evolution, find a lab with fruit flies or get one of the many nice programs that let undergrads play around with genetic drift.

michaeld, I did not say that evolution cannot take place without selection. You didn’t see that I am talking about the evolution of something specific (complex traits), rather than just “evolving populations”? I do know of neutral evolution, drift, and empirical examples of how they affect evolution. Above I was talking specifically about the evolution of complex traits (not about ‘complexity’ in general).

The eye-example you give says nothing about an increase in complexity of that trait. And I don’t think complexity has increased by any sensible measure.

Complexity increased at gene duplication as well as when the second gene changed function.

I is less complex then X. If I take that diagram on the photo on your blog and add an connection between the one of the blue connected dots and connect it to a green connected dot I’ve just made the diagram more complex.

Also by definition since evolution changes in alleles and alleles are changes in genes that code for proteins, then all alleles have a function (to code for a specific form of a gene (there are of course knock outs etc)).

The argument here isn’t that there is no selection, in PZ’s example he mentions several times sources of selection, its that genetic drift and chance can have a stronger affect on the evolution of a gene/trait then the selection forces.

Instead of a deleterious mutation well copy Pz’s example. Duplicate the last enzyme in a chain of eye pigment creating enzymes, then a chance functional mutation that changes the active site so that it now catalyzes a slightly different chemical reacting in the eye pigment (instead of catalyzing the forming of a C-C bond to C6 it forms one at a very similarly structured area at C20).

Now you have a an increase in the over all complexity of the system of eye pigment genes as well as a change in the complexity of the eye pigment if the eye pigment if the enzymes work sequentially such that the additions occur at C6 ad C20. Depending on the mutations the enzyme its self may have a more complex hold on the substrate because the mutation causes a slight change in the enzymes protein folding which now causes 2 new hydrogen bonds to form during the intermediary state.

I is less complex then X. If I take that diagram on the photo on your blog and add an connection between the one of the blue connected dots and connect it to a green connected dot I’ve just made the diagram more complex.

Increases complexity (depending on definition) of the genome, but not of any trait.

Also by definition since evolution changes in alleles and alleles are changes in genes that code for proteins, then all alleles have a function (to code for a specific form of a gene (there are of course knock outs etc)).

That a gene is expressed doesn’t mean it has function in terms of the phenotype, which is crucial if you are talking about traits.